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METHODS: Sixty healthy Sprague-Dawley rats were randomly divided into 3 groups: 6 rats in normal control group, 6 rats in EGb treating normal IOP group, and the other 48 rats were established chronic high IOP models of rats by cauterizing two episcleral veins. Then 30 rats satisfying experimental level were selected and randomly divided into five groups: 6 rats in physiological brine treating group, and the other 24 rats were divided into four experimental groups according to the dose of EGb: group A, EGb 50mg/; group B, EGb 100mg/; group C, EGb 150mg/; and group D EGb 200mg/. After the treating time of 1 month, the rats were sacrificed on schedule. Flat preparation of whole retinaes was stained distinctively and neuron counting in retinal ganglion cell layer from both eyes of each rat were performed to evaluate neuron situation.

取健康SD大鼠60只，正常对照组和正常银杏叶治疗组各6只，其余48只采用烧烙法，烙闭大鼠左眼2条浅层巩膜静脉，制作大鼠持续性高眼压模型，从中选出眼压稳定在实验要求水平的大鼠30只，随机分为生理盐水组，治疗A组（每日EGb 50mg/kg）、治疗B 组（每日EGb 100mg/kg）、治疗C 组（每日EGb 150mg/kg）、治疗D 组（每日EGb 200mg/kg），治疗时间为1mo，处死大鼠后做视网膜全层铺片，对RGCL神经元做特异性染色后行神经元计数分析来评估神经元的情况。

METHODS: Sixty healthy Sprague-Dawley rats were randomly divided into 3 groups: 6 rats in normal control group, 6 rats in EGb treating normal IOP group, and the other 48 rats were established chronic high IOP models of rats by cauterizing two episcleral veins. The n 30 rats satisfying experimental level were selected and randomly divided into five groups: 6 rats in physiological brine treating group, and the other 24 rats were divided into four experimental groups according to the dose of EGb: group A, EGb 50mg/; group B, EGb 100mg/; group C, EGb 150mg/; and group D EGb 200mg/. After the treating time of 1 month, the rats were sacrificed on schedule. Flat preparation of whole retinaes was stained distinctively and neuron counting in retinal ganglion cell layer from both eyes of each rat were performed to evaluate neuron situation.

取健康SD大鼠60只，正常对照组和正常银杏叶治疗组各6只，其余48只采用烧烙法，烙闭大鼠左眼2条浅层巩膜静脉，制作大鼠持续性高眼压模型，从中选出眼压稳定在实验要求水平的大鼠30只，随机分为生理盐水组，治疗A组（每日EGb 50mg/kg）、治疗B 组（每日EGb 100mg/kg）、治疗C 组（每日EGb 150mg/kg）、治疗D 组（每日EGb 200mg/kg），治疗时间为1mo，处死大鼠后做视网膜全层铺片，对RGCL神经元做特异性染色后行神经元计数分析来评估神经元的情况。

METHODS: Sixty healthy Sprague-Dawley rats were randomly divided into 3 groups: 6 rats in normal control group, 6 rats in EGb treating normal IOP group, and the other 48 rats were established chronic high IOP models of rats by cauterizing two episcleral veins. n 30 rats satisfying experimental level were selected and randomly divided into five groups: 6 rats in physiological brine treating group, and the other 24 rats were divided into four experimental groups according to the dose of EGb: group A, EGb 50mg/; group B, EGb 100mg/; group C, EGb 150mg/; and group D EGb 200mg/. After the treating time of 1 month, the rats were sacrificed on schedule. Flat preparation of whole retinaes was stained distinctively and neuron counting in retinal ganglion cell layer from both eyes of each rat were performed to evaluate neuron situation.

取健康SD大鼠60只，正常对照组和正常银杏叶组各6只，其余48只采用烧烙法，烙闭大鼠左眼2条浅层巩膜静脉，制作大鼠持续性高眼压模型，从中选出眼压稳定在实验要求水平的大鼠30只，随机分为生理盐水组，治疗A组（每日EGb 50mg/kg）、治疗B 组（每日EGb 100mg/kg）、治疗C 组（每日EGb 150mg/kg）、治疗D 组（每日EGb 200mg/kg），治疗时间为1mo，处死大鼠后做视网膜全层铺片，对RGCL神经元做特异性染色后行神经元计数来评估神经元的情况。

Our result showed that P450scc expression was observed in hippocampus, habenular nucleus, neuron nucleus of thalamus and hypothalamus, and cerebral neocortex. The colocalization of P450scc and NeuN demonstrated that most of P450scc exist in neuron cell in these regions. In order to clarify the transcriptional regulation of CYP11A1 gene, established the transient SCC-iCre transgenic mice model by using R26R system to study the promoter activity of human CYP11A1 gene in the brain.

为了证明内生性P450scc在这些脑区的表现，本研究利用免疫组织染色分析，说明了在小鼠海马回结构，间脑内的上视丘疆核、视丘神经核、下视丘神经核，与新皮质等区域中皆可侦测到，且主要表现在神经细胞。

The morphous of fetal rat cortical neuron is almost intact.Discussion:1 .Establishment of AD cellular modelSince Yankner 1990 first confirmed toxic effect of synthetic Aβ on hippocamp neuron in rats,cellular model was broadly used for research of mechanism of neurotoxicity due to advantages of simplification and utility.

讨论： 1.AD细胞模型的制作自从1990年Yankner首先证实合成的Aβ对培养大鼠海马神经元有毒性作用以来，体外培养的细胞模型以其简便、实用的优点被广泛用来研究Aβ的神经毒性机制。

Results: Both Pur and Hup-A improved learning memory ability of I/R mice, the effect of Pur group was better and the effect of combination group was the most significant. Both Pur and Hup-A decreased neuron apoptosis and raised content of monoamine nervous transmitter of I/R mice. The cortex neuron apoptosis rate in combination group was lower than that in Hup-A group,the homovanillic acid level of cerebral cortex in combination group was higher than that of Pur group.

结果：Pur（120 mg/kg）或Hup-A（400 μg/kg）都可提高I/R小鼠的学习记忆成绩，Pur组的作用优于Hup-A组，联合用药组（Hup-A 200 μg/kg+Pur 60 mg/kg）作用最强；各用药组都可降低大脑皮层细胞凋亡率，升高大脑皮层某些单胺类递质水平，其中，联合用药组的大脑皮层细胞凋亡率低于Hup-A组，大脑皮层高香草酸水平高于Pur组。

Objective To summarize the clinical symptom and the medicative feature of motor neuron disease. And to analyze internal relationship between motor neuron disease and the theory of the correlation of spleen and kidney.

目的总结归纳运动神经元疾病的临床症候、治疗用药的特点及其与中医脾肾相关理论的内在关系。

In pure cultured neuron, the inhibitory effect of 0.5mmol/L L-NNA on theincrease of LDH leaking after exposure of H/R and SIN-1 had also no statistical significance, but it could inhibit significantly the above index in mixedly cultured cerebral cortex neuron and glia.

在单纯培养神经细胞中0.5mmol／LL－NNA对H／R＋SIN－1导致的LDH漏出率增加仍无显著抑制作用，但可显著抑制H／R引起的混合培养的神经细胞和神经胶质细胞的LDH漏出率。

recovery of occlusion support facilitated increase of neuron numbers, or improvement of neuron functions, and decrease of neuroglial cell numbers in correlated brain sections of the patients, which may help improve the functions of nervous system.

研究表明，咬合支持的丧失可以导致相关脑区神经组织和神经代谢物的改变，并且这些变化与以学习记忆等功能衰退为特征的神经系统疾病如老年性痴呆的研究结果部分趋于一致，提示我们要对咬合支持丧失的危害性进行更深入地研究。

Nerve grows factor and brain-derived neurotropic factor, as one of the important active molecules, belong to neurotrophic family, which can affect the development of neuron and prevent neuron from damage.

神经生长因子（Nerve grows factor，NGF）和脑源性神经生长因子(Brain-derived neurotropic factor，BDNF)属于神经营养素家族，是神经系统重要的活性分子之一，是中枢神经系统胆碱能神经元、周围神经系统交感神经元及感觉神经元发育、分化、功能活动必不可少的营养分子。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。